Cultured fetal human adrenocortical cells are being used to study the effects of treatment with 11 Beta-hydroxylated steroids on various cellular functions. 11 Beta-Hydroxylated steroids interact with mitochondrial cytochrome P-450 11 Beta, causing a loss of 11 Beta-hydroxylase activity. This loss is preventable by dimethyl sulfoxide, a scavenger of hydroxyl radicals, and by butylated hydroxyanisole, a terminator of lipid peroxidation. It therefore appears that 11 Beta-hydroxylated steroids interact with cytochrome P-450 11 Beta causing the release of an oxygen-derived free radical which then initiates lipid peroxidation. Cytochrome P-450 species including cytochrome P-450 11 Beta are inactivated or destroyed by lipid peroxidation. The induction of cytochrome P-450 11 Beta by ACTH, in the presence and absence of antioxidants, and under conditions of low and high oxygen concentration, is being studied. Induction is much better under conditions of low oxygen; at high oxygen conditions induction was improved by the addition of ascorbic acid, an antioxidant vitamin. Research is centering on the mechanisms of action of 11 Beta-hydroxylated steroids in causing loss of 11 Beta-hydroxylase activity and which antioxidants are effective in preventing this loss.